The aim of the proposal is to test the hypothesis that the visual responsiveness of second order vestibular nerons in the vestibular nuclei of the brainstem increases after bilateral labyrinthectomy. This is hypothesized to be a mechanism for the compensation that occurs following this lesion, viz., the attentuation of oscillopsia, ataxia, and incoordination of gaze. The hypothesis will be tested by combining behavioral and single-celled extracellular neurophysiological recordings in awake, unrestrained guinea pigs. The behavioral compensation will be ascertained by comparing the gains of optokinetically-induced eye- and head-turning responses (gaze) before, versus after a bilateral labyrinthectomy. Previous work has shown that the gain of vertical optokinetic nystagmus increases after this lesion. Simultaneously, the responses of single second order neurons in the vestibular nuclei will be quantified, in order to correlate them with changes of gaze both before and after the bilateral labyrinthectomy. We expect to gain insight into the neurophysiological basis of a behavioral plasticity, namely, the visual recalibration that must occur after vestibular input has been removed bilaterally. After a pre-motor, neurophysiological correlate of the compensation has been identified, further experiments could be performed to test whether there has been structural change, or a change in pharmacological responsiveness in the vestibular nuclei, which would indicate a localized sign of learning. Once identified, these loci could then be experimentally manipulated in order to gain further insight into the cellular and molecular mechanisms of this central nervous system plasticity.